1. Field of the Invention
The present invention relates generally to controlling congestive heart failure and, more particularly, to electrically controlling a dilated condition resulting from congestive heart failure.
2. Related Art
The heart pumps blood through a patient's body in order to carry oxygen to, and remove carbon dioxide from, cells located throughout the body. In a patient having a normal heart, the rate at which the blood is pumped through the body increases or decreases to accommodate changes in the physiological needs of the patient. That is, as the cells of the patient's body require more oxygen, the heart rate and/or stroke volume increases to pump more oxygen-rich blood to the cells. When insufficient oxygen is available from the lungs, the respiration rate may also increase to increase the rate of oxygen intake into the body. Conversely, as the demand for oxygen decreases, the heart rate decreases, providing less blood flow and, hence, less oxygen, to the cells.
During a heart cycle, deoxygenated, venous blood enters the right atrium of the heart via the inferior vena cava and the superior vena cava and, during diastole, flows to the right ventricle. The pulmonary artery then delivers blood ejected from the right ventricle into the lungs. The pulmonary vein carries oxygenated blood from the lungs to the left atrium of the heart. During diastole, oxygenated blood flows from the left atrium to the left ventricle, which is filled to its end diastolic volume (EDV). During systole the left ventricle ejects oxygenated blood into the aorta.
The ventricles are cone-shaped muscular chambers that continuously change their shape during the heart cycle. The proper functioning of each ventricle is critically related to its internal dimension, wall thickness and the electrical states of the myocytes. In a normal heart, the left ventricle empties between 56% and 78% of its volume in systole; that is, the stroke volume is between 56% and 78% EDV.
Congestive heart failure (CHF) is a condition in which the heart is unable to provide the necessary amount of oxygenated blood to the body. CHF may be caused by any number of conditions, including high blood pressure, heart valve defects, congenital heart defects, myocardial infarction, irregular heart beat or pulmonary disease. Generally, CHF leads to a progressive dilatation of the heart. This dilatation is typically preceded by compensatory hypertrophy of the heart, or a thickening of the walls of the heart in response to vascular, valvular, or other heart disease. Progressive dilation of the heart increases the risk of developing dilated cardiomyopathy, which is a condition where the ventricles of the heart are weakened to the extent that they contract with less-than-optimal force during systole. This reduction in the systolic function can cause diminished stroke volume and reduced cardiac output.
The more dilated the heart becomes, the less it is able to contract and pump blood from the left ventricle into the aorta. The blood remaining in the heart increases the end-diastolic pressure in the left or right ventricle and, over time, increases the end diastolic volume. The elevated diastolic pressure is also transmitted through the pulmonary vein or artery to the lungs increasing pulmonary capillary pressure. An increase in pulmonary capillary pressure, in turn, can lead to the filling of the lungs with fluid, known as pulmonary edema. With pulmonary edema, breathing becomes more difficult, resulting in dyspnea, orthopnea and/or tachypnea. Furthermore, elevated right ventricular diastolic pressure increases the systemic venous pressure, which leads to peripheral venous congestion and edema.
Another symptom of dilated cardiac myopathy is inadequate blood flow to vital organs due to decreased cardiac output. Resulting problems may include decreased cerebral blood flow, impairing central nervous system function; and reduced blood profusion of the liver and kidneys, impairing hebetic and renal function. If left untreated, the heart's function progressively deteriorates, ultimately resulting in death.
Current treatment of dilated cardiomyopathy generally includes drug treatment. Common treatments include the use of diuretics, digitalis and angiotensin-converting enzyme inhibitors and anticoagulants. However, drug treatment typically does not return the heart to its normal physiological state.
What is needed, therefore, is a system and method that controls the dilatative effects of congestive heart failure, returning the heart to a more normal physiological state without compromising cardiac output or increasing the metabolic needs of the heart. That is, what is needed is a technique that prevents dilation of the heart which leads to the heart's reduced work capacity.